Comparative genomic hybridization of esophageal and gastroesophageal adenocarcinomas shows consensus areas of DNA gain and loss

Christopher A. Moskaluk*, Jie Hu, Elizabeth J. Perlman

*Corresponding author for this work

Research output: Contribution to journalArticle

71 Scopus citations

Abstract

Relatively little is known about the genetic changes that occur in esophageal and gastroesophageal adenocarcinomas. To provide a survey of relative DNA gains and losses in these cancers, we microdissected 15 primary human esophageal and gastroesophageal adenocarcinomas to enrich for cancer cells and subsequently performed comparative genomic hybridization. Eighteen regions of high-level amplification were detected in 11 tumors, with 8p23, 17q21, and 18p11 showing four, three, and two such events, respectively. The most common minimal regions of gain were 8q24 (8/15), 20q (7/15), 17q21 (7/15), and 7p11-15 (7/15). The most common minimal regions of loss were 5q12-21 (8/15), 4q 10-24 (5/15), 4p (5/15), and 18q (3/15). These results implicate the welt-characterized oncogenes MYC (8q24) and ERBB2 (17q21), and they predict the involvement of additional oncogenes on 8p23, 20q, and chromosome 7 in the pathogenesis of these cancers. Chromosomes 4 and 5 are frequent targets of deletion in these tumors and may harbor novel tumor suppressor genes.

Original languageEnglish (US)
Pages (from-to)305-311
Number of pages7
JournalGenes Chromosomes and Cancer
Volume22
Issue number4
DOIs
StatePublished - 1998

ASJC Scopus subject areas

  • Genetics
  • Cancer Research

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